Complex Regional Pain

PATHOPHYSIOLOGY

This is enigmatic; one CRPS theory suggests that cutaneous innervation is altered post-traumatically. Human pathologic studies demonstrate reduced local nociceptive fiber density with aberrant hair follicles and sweat glands innervation. However, it is not clear whether this is the primary pathology or a reaction to the painful symptoms.

Other studies propose that some central and peripheral sensitization leads to CRPS. Hyperalgesia and allodynia encountered after initial tissue trauma are attributed to local release of pronociceptive neuropeptides, leading to enhanced nociceptor responsiveness with lowered thresholds for innocuous thermal and mechanical stimuli. Higher preoperative pain intensity may predict postoperative CRPS invoking a central sensitization theory. Neuropeptides and proinflammatory cytokines released from injured nociceptive fibers are implicated in experimental neurogenic inflammation. Neuropeptides, such as calcitonin gene–related peptide (CGRP), substance P, and bradykinin, cause vasodilation, increase vessel permeability, hyperhidrosis, and hair growth in the affected area, leading to characteristic CRPS features.

Sympathetic nervous system dysfunction (SNSD) may account for common autonomic CRPS features. Reduced SNS-induced vasoconstriction predicts CRPS and explains the warm, red extremity in acute CRPS. Concomitantly, SNSD may contribute to post-traumatic nociceptive excitation through adrenergic receptors expressed on nociceptive fibers.

In addition, the central nervous system (CNS) may have a CRPS pathophysiologic role. The region of somatosensory cortex representing the affected limb is considerably reduced. Such brain plasticity is associated with greater pain intensity, hyperalgesia, and impaired tactile discrimination. Motor dysfunction accompanying CRPS may be linked to significant reorganization of central motor circuits.

CLINICAL FEATURES AND DIAGNOSIS

CRPS occurs predominantly with fractures and various surgeries, including total knee replacement, hip arthroplasty, carpal tunnel release, and numerous arthroscopic procedures. Major clinical CRPS features include spontaneous pain, allodynia, hyperalgesia, edema, vasomotor instability, autonomic dysfunction, and progressive trophic changes. CRPS pain occurs in a distribution beyond an initially affected nerve(s); eventually, this may involve the entire affected limb, and rarely, the contralateral limb. Weakness and tremor may occur, leading to profound functional loss. CRPS occurs as two subtypes: type I CRPS has no identifiable focal nerve lesion, often developing after minor fracture or trauma, whereas type II CRPS has specific nerve damage.

CRPS is diagnosed by clinical evaluation; there are no specific widely recognized diagnostic tests. Various diagnostic tools have their advocates, but the diagnosis remains clinical. Sympathetic nerve blocks at various levels of the neuraxis are sometimes used to support the presence of an autonomic component. If successful (>50% reduction in pain intensity), a more durable blockade with phenol or a radiofrequency ablation procedure may be performed.

TREATMENT

A multidisciplinary approach is used. Early diagnosis and prompt treatment favorably influence prognosis. Symptom management is based on pain severity. Physiotherapy, including range-of-motion exercise, desensitization, and isometric strengthening, is a first-line treatment.

Pharmacotherapy may begin with tricyclic antidepressants and antiepileptics; although these are effective in treating neuropathic pain, their usefulness in CRPS patients is not precisely defined. Anti-inflammatory drugs, including nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids are sometimes effective. Topical analgesic using capsaicin and lidocaine transdermal patches is sometimes effective. Opioids are sometimes valuable when tolerated because these analgesics have demonstrated efficacy for neuropathic pain, but adverse consequences, such as tolerance, abuse, and misuse, may become problematic.

A number of interventional modalities exist. Those used include regional anesthetic blocks (i.e., sympathetic blockade), sympathectomy, and somatic blockade when moderate-to-severe pain does not respond to physiotherapy or pharmacotherapy. Neuromodulation, such as transcutaneous electrical nerve stimulation (TENS) at the site of the pain and spinal cord stimulation (SCS), has also shown promise in the treatment of CRPS, and a subpopulation of patients may experience a durable robust response. These modalities are demanding to perform and require a pain medicine specialist.

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